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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Maas, C. Tromp, J. M. Van Laar, J. Thijssen, R. Elias, J. A. Malara, A. Krippner-Heidenreich, A. Silke, J. Van Oers, M. Hj Eldering, E. |
| Description | Country affiliation: Netherlands Author Affiliation: Maas C ( Department of Hematology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.) |
| Abstract | In the lymph node (LN) environment, chronic lymphocytic leukemia (CLL) cells display increased NF-κB activity compared with peripheral blood CLL cells, which contributes to chemoresistance. Antagonists of cellular inhibitor of apoptosis proteins (cIAPs) can induce apoptosis in various cancer cells in a tumor necrosis factor- (TNF )-dependent manner and are in preclinical development. Smac-mimetics promote degradation of cIAP1 and cIAP2, which results in TNFR-mediated apoptosis via formation of a ripoptosome complex, comprising RIPK1, Fas-associated protein with death domain, FLICE-like inhibitory protein and caspase-8. CD40 stimulation of CLL cells in vitro is used as a model to mimic the LN microenvironment and results in NF-κB activation and TNF production. In this study, we investigated the response of CLL cells to smac-mimetics in the context of CD40 stimulation. We found that treatment with smac-mimetics results in cIAP1 and cIAP2 degradation, yet although TNF is produced, this did not induce apoptosis. Despite the presence of all components, the ripoptosome complex did not form upon smac-mimetic treatment in CLL cells. Thus, CLL cells seem to possess aberrant upstream NF-κB regulation that prevents ripoptosome formation upon IAP degradation. Unraveling the exact molecular mechanisms of disturbed ripoptosome formation may offer novel targets for treatment in CLL. |
| File Format | HTM / HTML |
| e-ISSN | 20414889 |
| DOI | 10.1038/cddis.2013.305 |
| Journal | Cell Death and Disease |
| Volume Number | 4 |
| Language | English |
| Publisher | Nature Publishing Group |
| Publisher Date | 2013-08-29 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | 3t3 Cells Research Support, Non-u.s. Gov't Intracellular Signaling Peptides And Proteins Multiprotein Complexes Gene Expression Regulation, Neoplastic Drug Resistance, Neoplasm Biosynthesis Proteasome Endopeptidase Complex Antigens, Cd40 Proteolysis Cell Death Genetics Nf-kappa B Piperazines Signal Transduction Inhibitor Of Apoptosis Proteins Receptors, Tumor Necrosis Factor, Type I Cd40 Ligand Pharmacology Metabolism Biphenyl Compounds Drug Effects Tumor Necrosis Factor-alpha Discipline Cell Biology Pathology Animals Sulfonamides Receptors, Tumor Necrosis Factor, Type Ii Mice Nitrophenols Mutation Leukemia, Lymphocytic, Chronic, B-cell Ubiquitin-protein Ligases |
| Content Type | Text |
| Resource Type | Article |
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